| 2000 |
KIF17 directly interacts with the PDZ domain of mLin-10 (Mint1/X11) via its tail domain, linking it to a large protein complex (mLin-2/CASK, mLin-7/MALS/Velis, NR2B) to transport NR2B-containing vesicles along microtubules in neuronal dendrites. |
Co-immunoprecipitation, direct binding assay (tail-PDZ interaction), vesicle transport reconstitution in neurons |
Science |
High |
10846156
|
| 2003 |
KIF17 vesicles move processively along dendrites at ~0.76 µm/sec and are associated with extrasynaptic NR2B; knockdown or dominant-negative blockade of KIF17 reduces NR2B expression and its synaptic localization, accompanied by a compensatory increase in synaptic NR2A. |
Live-cell imaging of GFP-tagged KIF17 in hippocampal neurons, siRNA knockdown, dominant-negative overexpression, immunostaining |
The Journal of Neuroscience |
High |
12514209
|
| 2002 |
Overexpression of KIF17 in transgenic mice upregulates NR2B expression and increases CREB phosphorylation, demonstrating that KIF17 motor activity drives in vivo NR2B transport and influences downstream transcriptional programs linked to learning and memory. |
Transgenic mouse overexpression (GFP-KIF17), behavioral assays, Western blot, CREB phosphorylation analysis |
PNAS |
High |
12391294
|
| 2007 |
CaMKII phosphorylates KIF17 at Ser1029 in its tail domain, disrupting the KIF17–Mint1 interaction and releasing transported NR2B-containing cargo from the motor. |
FRET (direct visualization of protein-protein interaction), in vitro kinase assay, site-directed mutagenesis, co-immunoprecipitation |
Nature Cell Biology |
High |
18066053
|
| 2011 |
Genetic deletion of kif17 in mice impairs NR2B transport and reduces nr2b transcription; it also reduces NR2A levels via accelerated ubiquitin-proteasome degradation. Synaptic NMDAR-mediated currents, LTP, LTD, CREB responses, and hippocampus-dependent memory are all attenuated in kif17−/− mice. |
Kif17 knockout mouse, electrophysiology, behavioral testing, Western blot, ubiquitin-proteasome inhibitor rescue experiments |
Neuron |
High |
21521616
|
| 2012 |
Phosphorylation of KIF17 at Ser1029 by CaMKII is required bidirectionally for normal NR2B transport in vivo: phospho-null (S1029A) mice cannot load GluN2B cargo onto KIF17, while phospho-mimetic (S1029D) mice cannot unload it; both result in reduced synaptic NMDA receptors, impaired synaptic plasticity, and spatial memory deficits. |
Transgenic mice expressing S1029A or S1029D KIF17 in kif17−/− background, electrophysiology, behavioral assays, immunostaining |
The Journal of Neuroscience |
High |
22514311
|
| 2010 |
KIF17 contains a ciliary localization signal (CLS) in its tail domain that is necessary and sufficient for ciliary targeting. The CLS is recognized by importin-β2, and this interaction is inhibited by RanGTP. Cytoplasmic expression of GTP-locked Ran(G19V) abolishes ciliary entry of KIF17, establishing that a Ran-GTP gradient (analogous to nuclear import) regulates KIF17 ciliary entry. |
CLS deletion/fusion constructs, importin-β2 co-immunoprecipitation, dominant-negative RanG19V expression, live-cell imaging |
Nature Cell Biology |
High |
20526328
|
| 2006 |
KIF17 is required for ciliary targeting of olfactory CNG channels in mammalian olfactory sensory neurons; dominant-negative KIF17 disrupts CNG channel localization to olfactory cilia. |
Dominant-negative KIF17 expression, immunofluorescence in olfactory sensory neurons |
Current Biology |
Medium |
16782012
|
| 2006 |
In C. elegans, OSM-3 (KIF17 ortholog) and kinesin-II cooperate via a mechanical competition mechanism to move IFT particles along microtubule doublets; purified OSM-3 and kinesin-II alone can recapitulate cooperative movement in vitro without additional regulatory factors. |
Competitive in vitro MT gliding assays with purified motors, in vivo IFT transport assays in BBS and motor mutants, quantitative modeling |
The Journal of Cell Biology |
High |
17000880
|
| 2006 |
OSM-3 (C. elegans KIF17 ortholog) motility is autoinhibited in solution via intramolecular folding at a central hinge; a G444E point mutation in the hinge or hinge deletion relieves autoinhibition, activating ATPase and processive movement. Cargo attachment (bead in optical trap) also activates wild-type OSM-3 motility. |
Single-molecule fluorescence assay, MT-stimulated ATPase assay, optical trap, site-directed mutagenesis (G444E), EM/conformational analysis |
The Journal of Cell Biology |
High |
17000874
|
| 2016 |
Polarized dendritic sorting of KIF17 requires three steps: (1) cargo binding relieves KIF17 autoinhibition and initiates microtubule transport; (2) the actin cytoskeleton at the axon initial segment (AIS) acts as a filter preventing KIF17-coupled vesicles from progressing into the axon; (3) dynein-based activity redirects KIF17 cargo into dendrites. |
Live-cell imaging, inducible trafficking assays (rapamycin-based), actin depolymerization, dynein inhibition in cultured neurons |
Current Biology |
High |
27265394
|
| 2008 |
KIF17 (zebrafish Kif17) is essential for photoreceptor outer segment (OS) development; Kif17 knockdown severely disrupts OS formation and visual pigment targeting. Kif17 co-immunoprecipitates with IFT proteins within photoreceptor OS, establishing it as part of the IFT machinery in vertebrate photoreceptors. |
Morpholino knockdown in zebrafish, co-immunoprecipitation with IFT proteins, immunofluorescence |
Developmental Biology |
High |
18304522
|
| 2005 |
KIF17 transports the K+ channel Kv4.2 to dendrites; dominant-negative KIF17 (but not dominant-negatives of other kinesins) dramatically inhibits dendritic localization of endogenous and introduced Kv4.2. Kv4.2 and KIF17 co-immunoprecipitate from brain lysate and from co-transfected COS cells, indicating direct or indirect interaction through the extreme C-terminus of Kv4.2. |
Dominant-negative constructs, co-immunoprecipitation from brain lysate and COS cells, colocalization in cortical neurons |
The Journal of Biological Chemistry |
Medium |
16257958
|
| 2006 |
KIF17 interacts with kainate receptor subunits GluR6 and KA2 and is required for localization of GluR5 to distal dendrites; coimmunoprecipitation from hippocampal neurons and dominant-negative KIF17 experiments established this interaction and functional requirement. |
Co-immunoprecipitation from hippocampal neurons, dominant-negative KIF17 expression, immunofluorescence |
Molecular and Cellular Neurosciences |
Medium |
17174564
|
| 2005 |
KIF17b (testis-specific isoform) controls the subcellular localization of the CREM transcriptional coactivator ACT between nucleus and cytoplasm in a manner that is independent of its motor domain and microtubules but dependent on protein kinase A-mediated phosphorylation of KIF17b. |
Truncation/deletion constructs, microtubule depolymerization (nocodazole), PKA inhibitor/activator experiments, subcellular fractionation |
The Journal of Biological Chemistry |
Medium |
16002395
|
| 2003 |
KIF17b (testis-specific isoform) co-immunoprecipitates with TB-RBP (Translin) in an RNA-protein complex that contains specific CREM-regulated mRNAs, and KIF17b serves as the motor component transporting these mRNPs in postmeiotic male germ cells; dissociation of KIF17b and TB-RBP from mRNA is temporally linked to the time of translation. |
Co-immunoprecipitation, in vivo RNA-protein crosslinking, in situ hybridization combined with immunohistochemistry at EM level |
PNAS |
Medium |
14673085
|
| 2006 |
KIF17b physically interacts with the PIWI/Argonaute family protein MIWI in chromatoid bodies of round spermatids; KIF17b localizes to chromatoid bodies and may provide microtubule-dependent mobility to these structures and facilitate loading of haploid RNAs. |
Co-immunoprecipitation (KIF17b–MIWI), immunofluorescence localization, analysis of miwi-null mouse spermatids |
Journal of Cell Science |
Medium |
16787948
|
| 2017 |
KIF17 ciliary entry requires two independent determinants: (1) binding to the IFT46–IFT56 dimer of the IFT-B complex through a C-terminal sequence just upstream of the NLS, and (2) the NLS itself, to which importin-α proteins bind. KIF17 reaches the ciliary tip independently of its motor domain and is dispensable for ciliogenesis and IFT-B trafficking in mammalian cells. |
Visible immunoprecipitation (VIP) assay, deletion mutant analysis, importin-α co-immunoprecipitation, live-cell imaging of ciliary tip accumulation |
Molecular Biology of the Cell |
High |
28077622
|
| 2015 |
Ciliary delivery of D1-type dopamine receptors from the extra-ciliary plasma membrane requires IFT-B, KIF17, and Rab23; Rab23 depletion prevents receptor ciliary access, and fusion of Rab23 to a non-ciliary receptor drives nucleotide-dependent mis-localization to cilia. |
siRNA knockdown of IFT-B, KIF17, Rab23; constitutively active/dominant-negative Rab23 fusions; live-cell imaging of receptor trafficking |
eLife |
High |
26182404
|
| 2015 |
Rab23 forms a complex with KIF17 and importin-β2, and Rab23 depletion disrupts ciliary localization of KIF17; wild-type and constitutively active Rab23(Q68L) enrich at the primary cilium, suggesting Rab23 acts as an effector regulating KIF17 ciliary transport. |
Co-immunoprecipitation, affinity-binding assay (Rab23–KIF17–importin-β2 complex), siRNA knockdown, immunofluorescence |
Journal of Cell Science |
Medium |
26136363
|
| 2013 |
The KIF17 motor domain (K370) directly stabilizes microtubule plus-ends and inhibits depolymerization independently of EB1; the KIF17 autoinhibitory tail domain binds microtubules and tubulin dimers and delays initial MT polymerization. EB1 and the KIF17 tail competitively interact with the motor domain and have opposing effects on MT-stimulated ATPase activity. |
In vitro MT dynamic instability assay, MT-stimulated ATPase assay, MT dilution depolymerization assay, MT cosedimentation, nocodazole washout in cells |
The Journal of Biological Chemistry |
High |
24072717
|
| 2016 |
KIF17 localizes at epithelial cell-cell adhesions where it activates RhoA signaling through its motor domain (independently of microtubule binding), promoting junctional actin accumulation via the RhoA–ROCK–LIMK–cofilin pathway and stabilizing the apical junctional complex. |
KIF17 depletion (siRNA), overexpression of full-length and truncation mutants, dominant-negative RhoA, ROCK inhibitor, kinase-dead LIMK1, activated cofilin(S3A), GFP-actin incorporation assay, 3D organotypic culture |
Journal of Cell Science |
High |
26759174
|
| 2016 |
Septin 9 (SEPT9) directly associates with the C-terminal tail of KIF17 (preferentially in the extended cargo-binding conformation), competes with the PDZ1 domain of mLin-10/Mint1 for KIF17 tail binding, and thereby down-regulates NR2B transport into hippocampal neuron dendrites without affecting KIF17 microtubule-based motility. |
Direct binding assay (GST pulldown with purified proteins), co-immunoprecipitation, live-cell imaging of KIF17 motility, NR2B immunostaining in neurons, siRNA knockdown |
Molecular Biology of the Cell |
High |
26823018
|
| 2013 |
TTC30B (mouse ortholog of C. elegans DYF-1) interacts directly with KIF17 as shown by co-immunoprecipitation and cell-free in vitro expression co-IP, and also associates with multiple IFT-B complex proteins, suggesting a physical link between TTC30B and KIF17 within the IFT machinery. |
Co-immunoprecipitation from mouse pituitary cells, in vitro cell-free expression followed by Co-IP, mass spectrometry |
Experimental Cell Research |
Medium |
23810713
|
| 2018 |
CaMKII-dependent phosphorylation of KIF17 at Ser815 (zebrafish equivalent of mouse Ser1029) promotes KIF17 localization along cone outer segments and drives outer segment disc shedding in a cell-autonomous manner; kif17 genetic mutants in zebrafish and mice exhibit diminished disc shedding, and constitutively active CaMKII increases disc shedding in a kif17-dependent manner. |
Transgenic zebrafish expressing phospho-mimetic/phospho-null KIF17, kif17 genetic mutants in zebrafish and mice, constitutively active CaMKII transgene, quantitative disc shedding assay |
BMC Cell Biology |
High |
30458707
|
| 2019 |
GTP-bound Rab23 promotes migration of Kif17 to spindle poles during mouse oocyte meiosis. Depletion of Rab23 or Kif17 causes polar body extrusion failure, perturbs spindle formation, and disrupts tubulin acetylation via altered αTAT and Sirt2 expression. The Kif17 tail domain associates with constituents of the RhoA–ROCK–LIMK–cofilin pathway to regulate cytoplasmic actin and spindle migration. |
siRNA depletion of Rab23 and Kif17 in mouse oocytes, immunofluorescence for spindle markers, Western blot for αTAT/Sirt2, Co-immunoprecipitation of Kif17 tail with RhoA pathway components |
Development |
Medium |
30696709
|
| 2020 |
KIF17 is locally degraded and synthesized in dendrites in an NMDAR-activity-dependent manner; activity-dependent local synthesis is driven by the KIF17 3'UTR at dendritic shafts, and newly synthesized KIF17 engages in dendritic transport. Hippocampus-specific deletion of Kif17 3'UTR impairs fear memory extinction by disrupting activity-dependent KIF17 synthesis. |
Live imaging of GFP-KIF17 synthesis in dendrites, 3'UTR reporter assays, NMDAR antagonist/agonist treatments, hippocampus-specific 3'UTR deletion mouse, fear conditioning and extinction behavioral assay |
Science Advances |
High |
33328231
|
| 2021 |
Crystal structures of the OSM-3 (C. elegans KIF17 ortholog) motor domain in ADP-bound, nucleotide-free, and ATP-analog-bound states show that the nucleotide-binding site is virtually identical to that of Eg5 in the ATP-like state, demonstrating that a two-water-molecule ATP hydrolysis mechanism is conserved in kinesin-2. |
X-ray crystallography (structures 7A3Z, 7A40, 7A5E), structural comparison with Eg5 |
FEBS Open Bio |
High |
33513284
|
| 2017 |
KIF17 interacts with estrogen-related receptor alpha (ERRα) via its C-terminal tail (containing an LXXLL nuclear receptor box) and the ERRα ligand-binding/AF2 domain; KIF17 tail expression attenuates nuclear accumulation of newly synthesized ERRα and inhibits ERRα transcriptional activity, while KIF17 knockout elevates ERRα activity. |
Yeast-2-hybrid screen, in vitro binding assay, KIF17 knockout cells, nuclear fractionation, reporter gene (transcriptional activity) assay, deletion/peptide constructs |
Oncotarget |
Medium |
28881568
|
| 2024 |
KIF17 has dual and opposing roles in Hedgehog (HH)-dependent cerebellar development: in Purkinje cells (HH-producing), KIF17 promotes SHH protein levels and its cell-type-specific deletion reduces SHH and CGNP proliferation; in CGNPs (HH-responding), KIF17 deletion increases CGNP proliferation and HH target gene expression by altering GLI transcription factor processing. |
Germline Kif17 knockout mice, Purkinje cell-specific and CGNP-specific conditional Kif17 deletion, cerebellar morphometry, HH pathway target gene expression (qPCR/Western blot), GLI processing analysis |
Science Advances |
High |
38669326
|
| 2025 |
In C. elegans, NEKL-3 (a NIMA-related kinase) directly phosphorylates the motor domain of OSM-3 (KIF17 ortholog), inhibiting its in vitro ATPase activity; NEKL-3 and NEKL-4 localize at the ciliary base and restrict OSM-3 activation to the distal ciliary region. Elevated protein phosphatase 2A at the transition zone triggers premature OSM-3 activation, while PP2A deficiency reduces OSM-3 activity and cilia length. |
In vitro kinase assay (NEKL-3 phosphorylation of OSM-3), fluorescence lifetime imaging microscopy (FLIM) for OSM-3 conformational state in vivo, genetic analysis of NEKL-3/4 and PP2A mutants, FRAP |
The Journal of Cell Biology |
High |
40272473
|
| 1993 |
osm-3 encodes a kinesin heavy chain-like protein with conserved ATPase and microtubule-binding domains; osm-3 mutants accumulate dense matrix material in amphid sheath cytoplasm and have shortened distal cilia segments, establishing a kinesin-like role in axonal/ciliary transport in C. elegans chemosensory neurons. |
Germline transformation rescue, DNA sequencing, Northern blot, electron microscopy of cilia ultrastructure |
Neuroreport |
Medium |
7690265
|
| 2022 |
KIF17 is modified by SUMOylation, which stabilizes and maintains KIF17 protein levels in epileptic neurons; KIF17 overexpression increases severity of KA-induced epileptic activity and elevates membrane NR2B expression, while KIF17 knockdown has the opposite effect. |
KIF17 overexpression/knockdown in mouse epilepsy model, SUMO modification assay, electrophysiology, NR2B membrane fractionation |
Neuroscience Bulletin |
Medium |
35678994
|
| 2010 |
Nuclear respiratory factor 1 (NRF-1) directly binds conserved sites in the Kif17 gene promoter and functionally regulates Kif17 transcription; NRF-1 silencing blocks KCl-depolarization-induced Kif17 upregulation, while NRF-1 overexpression rescues TTX-suppressed Kif17 expression, co-regulating KIF17 with its cargo NR2B. |
EMSA, supershift assay, chromatin immunoprecipitation (ChIP), promoter mutation assay, NRF-1 siRNA knockdown and overexpression, real-time qPCR |
Biochimica et Biophysica Acta |
High |
21171239
|